latheo, a Drosophila gene involved in learning, regulates functional synaptic plasticity
latheo, a Drosophila gene involved in learning, regulates functional synaptic plasticity
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DOI：
10.1016/s0896-6273(00)80753-9
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发表时间：
1999-05-01
期刊：
影响因子：
16.2
通讯作者：
Broadie, K
中科院分区：
文献类型：
--
作者：
Rohrbough, J;Pinto, S;Broadie, K
Latheo（laf）基因突变会破坏果蝇的联想学习，但LAT在调节神经元功能中的作用尚未得到证实。在这里，我们报告说，LAT在调节钙离子和活性依赖性突触可塑性中起着核心作用。LAT蛋白的免疫定位表明，它存在于幼虫神经肌肉接头（NMJ）的突触连接，并在突触前终扣富集。在laf突变NMJ的基础突触传递振幅升高3至4倍，和Ca2+依赖性的传输显着降低。多种形式的突触易化和强直后增强（PTP）在突变突触中被强烈抑制或缺失。我们的研究结果表明，LAT是一种新的突触前蛋白的Ca 2+依赖性突触调制机制的作用，行为可塑性。
Mutations in the latheo (laf) gene disrupt associative learning in Drosophila, but a role for LAT in regulating neuronal function has not been demonstrated. Here, we report that LAT plays a central role in regulating Ca2+- and activity-dependent synaptic plasticity. Immunological localization of the LAT protein indicates it is present at synaptic connections of the larval neuromuscular junction (NMJ) and is enriched in presynaptic boutons. Basal synaptic transmission amplitude at the laf mutant NMJ is elevated 3- to 4-fold, and Ca2+ dependence of transmission is significantly reduced. Multiple forms of synaptic facilitation and posttetanic potentiation (PTP) are strongly depressed or absent at the mutant synapse. Our results suggest that LAT is a novel presynaptic protein with a role in the Ca2+-dependent synaptic modulation mechanisms necessary for behavioral plasticity.